Typical gait analysis devices and methods can provide overall evaluation of motor impairment due to disease or trauma. An example of an existing system can be obtained from Noldus (http://www.noldus.com/CatWalk-XT/) for $48,170, which may include analysis software and a device. The Noldus CatWalk™ XT may be based on the Ladder Run Walking test or task, which can include: 1) footprint outline (print area, stand index, intensity); 2) distances between footprints (base of support, stride length); and, 3) time relationships between footprints (cadence, support and swing duration). The device may automatically detect the timing of gait phases in self-paced locomotion. Noldus CatWalk™ XT software may further provide qualitative and quantitative analysis of individual footfall parameters. Yet, one deficiency exhibited by this and similar systems is the lack of capability to instruct animals about a desired pattern of locomotion.
The Ladder Rung Walking task/test had been developed for mice (Farr: 2006) and for rats (Metz: 2009) to test the control of paw placement that had been impaired after suffering damage to the corticospinal pathways. The task/test tends to rely on methods to impose bilateral pattern of locomotion without any means to control which limb is used to step on rungs. For reasons explained below, this can lead to deficiencies in existing gait analysis devices and methods.
Behavioral assays can be used for assessing sensorimotor impairment in the central nervous system (CNS). One of the more sophisticated methods for quantifying locomotor deficits in rodents can be to measure minute disturbances of unconstrained gait overground (e.g. manual the Basso, Beattie, and Bresnahan (BBB) locomotor scale or automated CatWalk). However, cortical inputs are not required for generation of basic locomotion produced by the spinal central pattern generator (CPG). Thus, unconstrained walking tasks, such as those relied upon by existing gait devices and methods, only indirectly test for locomotor deficits caused by motor cortical impairment.
Post-stroke morbidity in a surviving population may include gross motor impairments that can pose a challenge for quantitative evaluation in both post-stroke humans and animal models of neurologic impairment.1 For example, in a clinical setting, these motor impairments are typically measured using subjective criteria, which tend to be more sensitive to severe impairment rather than moderate impairment. Yet, a majority of surviving patients exhibit moderate impairment as opposed to severe impairment. In addition, assessments of post-injury motor behavior in animals commonly use subjective assessment techniques (e.g. BBB locomotor scale method) to generate the subjective criteria alluded to above.2,3 While these subjective evaluation methods may assist with translation between gait rehabilitation studies in quadruped animal models and humans, such methods may not be as effective for assessing details of motor deficits associated with activity of separate muscle groups. This is compounded with the fact that the assessment of motor cortical contribution to locomotion (the putative culprit of motor deficit in cerebrovascular accident) may only be obtained indirectly when using such techniques, even when employing advanced automated quantitative methods.4,5 Again, this can be due to such techniques' heavy reliance on open-field or linear walking tasks.
Open-field or linear walking tasks may not require cortical contribution, and thus can be performed by the neural mechanisms of the spinal cord, i.e. the CPG network. Yet, the CPG network is typically spared in most animal models of neural damage, e.g. spinalized animals6-8. This is in spite of the fact that essential cortical contribution to these spinal mechanisms had been experimentally implicated in tasks that require anticipated postural adjustments9 and reaching10, as well as precise stepping10.
Moreover, most neurological damage is asymmetric. For example, stroke generally causes hemiparesis, e.g. weakness on one side of the body, which can result in an asymmetric gait.11-14 The asymmetry of hemiplegic gait can be produced by asymmetric spatiotemporal muscle activation most significantly manifested in the shortening of the extensor-associated stance phase and the lengthening of the flexor-associated swing phase of the step cycle on the paretic side.15,16 This trend has not yet been explored across a range of locomotor speeds in healthy or paretic animals.
The present invention is directed toward overcoming one or more of the above-identified problems.